Type 2 diabetes (T2D) has been suggested to be both a metabolic and inflammatory disease. Metformin is a metabolic modulator and widely used as first-line therapy for T2D. When TCA cycle is broken, the metabolic intermediate succinate could act as the inflammatory signal to induce the production of IL-1β, whereas metformin could reduce TCA cycle activity. Recent studies have demonstrated the therapeutic effects of the mesenchymal stem cells (MSCs) on T2D by preventing β cells from immune cell attack. Combined metformin and MSCs could be a possible choice to treat T2D. In this study, we investigated the immunomodulation of metformin on the MSCs, including clarifying the role of succinate in the mechanisms. Our results demonstrated the immunosuppressive function of 1mM metformin- or succinate-treated MSCs by culturing with T cell. In addition, we also evaluated the differentiation ability of metformin- or succinate-treated MSCs. Treatment of MSCs in differentiation medium with 0.5mM/1mM metformin or succinate lead to an increased differentiation of adipocyte in metformin but a decreased in the culture succinate. In the study, we will further assay the cytokines and metabolic changes of MSCs after treatment with metformin and succinate. We believe further clarification on the metabolic mechanisms involved in the development and functions of MSCs might shed light on future application of MSCs for immune modulation.